The objective of this investigation is to test the hypothesis that progressive massive fibrosis of the lungs (PMF) is the result of an altered inflammatory response of lung tissue caused by an induced hypersensitivity. The latter is thought to be accentuated by adsorption of antigen to the stored dust in the lungs, which prevents the destruction of the antigen and favors prolongation of its activity. The method of attack is to produce PMF in guinea pigs by rendering them hypersensitive as judged by a positive skin test and then, by means of a large pulmonary burden of coal dust with adsorbed antigen, producing pneumoconiosis. It is to be emphasized that this investigation does not propose to analyze the immunological mechanisms involved, but rather to study the morphogenesis of PMF.